Interfacial tensions of 10 normal alkane + water/brine and hydrocarbon mixture + water/brine systems were measured by using a pendent drop instrument. The temperature and pressure ranges of measurements are (25 to 80) °C and (1 to 300) bar, respectively. The effects of temperature, pressure, and salt content have been studied. It was found that the interfacial tension is sensitive to temperature and salt concentration but weakly dependent on pressure and salt species.
Background The role of Berberine (BBR) in colorectal cancer (CRC) and gut microbiota has begun to appreciate. However, there was no direct evidence confirm that the gut microbiota regulated by BBR could inhibit CRC. This report investigated the effect of stool from BBR treated subjects and its effect on CRC. Methods A mouse model for CRC was developed using azoxymethane (AOM) and dextran sulfate sodium (DSS). Intestinal tissue from affected mice were used to determine the efficacy of BBR against CRC. Stool samples were collected for the 16s rRNA gene sequencing and fecal microbiota transplantation (FMT). Finally, the mechanism of gut microbiota from BBR treated mice on CRC was explored using immunohistochemistry, RNA-Sequencing, quantitative RT-PCR, and western blot analyses. Results BBR significantly reduced intestinal tumor development. The richness of gut microbiota were notably decreased by BBR. Specifically, the relative abundance of beneficial bacteria (Roseburia, Eubacterium, Ruminococcaceae, and Firmicutes_unclassified) was increased while the level of bacteria (Odoribacter, Muribaculum, Mucispirillum, and Parasutterella) was decreased by BBR treatment. FMT experiment determined that the mice fed with stool from BBR treated AOM/DSS mice demonstrated a relatively lower abundance of macroscopic polyps and a significantly lower expression of β-catenin, and PCNA in intestinal tissue than mice fed with stool from AOM/DSS mice. Mechanistically, intestinal tissue obtained from mice fed with stool from BBR treated AOM/DSS mice demonstrated a decreased expression of inflammatory cytokines including interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α), C-C motif chemokine 1 (Ccl1), Ccl6, and C-X-C motif ligand (Cxcl9). In addition, the NF-κB expression was greatly suppressed in mice fed with stool from BBR treated AOM/DSS mice. Real-time PCR arrays revealed a down-regulation of genes involved in cell proliferation, angiogenesis, invasiveness, and metastasis in mice fed with stool from BBR treated AOM/DSS mice. Conclusions Stool obtained from BBR treated AOM/DSS mice was able to increase colon length while simultaneously decreasing the density of macroscopic polyps, cell proliferation, inflammatory modulators and the expression of NF-κB. Therefore, it was concluded that suppression of pro-inflammatory genes and carcinogens factors by modulating gut microbiota was an important pathway for BBR to inhibit tumor growth in conventional mice.
Although first-line chemotherapy drugs, including 5-fluorouracil (5-FU), remain one of the major choice for cancer treatment, the clinical use is also accompanied with dose-depending toxicities, such as intestinal mucositis (IM), in cancer patients undergoing treatment. IM-induced gastrointestinal adverse reactions become frequent reason to postpone chemotherapy and have negative impacts on therapeutic outcomes and prognosis. Various studies have evidenced the anticancer role of curcumin in many cancers; except for this effect, studies also indicated a protective role of curcumin in intestinal diseases. Therefore, in this study, we investigated the effect of curcumin on inflammation, intestinal epithelial cell damage in an IM model. 5-FU was used to induce the model of IM in intestinal epithelial cells, and curcumin at different concentrations was administrated. The results showed that curcumin efficiently attenuated 5-FU-induced damage to IEC-6 cells, inhibited the levels of inflammatory cytokines, attenuated the 5-FU-induced inhibition on cell viability, and displayed antiapoptosis effect on IEC-6 cells. Further RNA-sequencing analysis and experiment validation found that curcumin displays its protective effect against 5-FU-induced IM in intestinal epithelial cells by the inhibition of IL-6/STAT3 signaling pathway. Taken together, these findings suggested that curcumin may be provided as a therapeutic agent in prevention and treatment of chemotherapy-induced IM.
The traditional Chinese medicine (TCM)–Chaihu Shugan Formula (CSF), consisting of several Chinese botanical drugs like Bupleurum, is derived from the ancient Chinese pharmacopeia. It has been used for more than thousands of years in various suboptimal health statuses and diseases induced by chronic stress based on empirical therapy. Recent studies confirm the role of CSF in the development of many diseases, including depression, stress-induced hepatic injury and tumors. However, little has been known about the mechanisms behind the health effects of CSF. Here, we investigate the influence of CSF on the modulation of the simulated colonic microbiota of five healthy donors, gut barrier integrity, and intestinal immunity by combining the simulator of the human intestinal microbial ecosystem (SHIME®) technology platform with co-culture of intestinal and immune cells. This approach revealed that CSF stimulated the production of SCFA (acetate, propionate and butyrate) across donors while significantly lowering the production of branched SCFA (bSCFA). In terms of community composition, CSF stimulated a broad spectrum of health-related Bifidobacterium species, which are potent acetate and lactate producers. At the same time, it lowered the abundance of opportunistic pathogenic Escherichia coli. Later, we explore the effect of colonic fermentation of CSF on the gut barrier and intestinal immunity in the Caco-2/THP1-blue™ cell co-culture model. Based on the study using SHIME technology platform, CSF showed protective effects on inflammation-induced intestinal epithelial barrier disruption in all donors. Also, the treatment of CSF showed pronounced anti-inflammatory properties by strongly inducing anti-inflammatory cytokines IL-6 and IL-10 and reducing pro-inflammatory cytokine TNF-α. These findings demonstrate a significant modulatory effect of CSF on intestinal gut microbiota. CSF-microbial fermentation products improved the gut barrier and controlled intestinal inflammation.
Background. With the increasing incidence of breast cancer and the integration of multiple methods in the treatment, traditional Chinese medicine plays an increasingly important role in the comprehensive treatment of breast cancer. we aimed to determine the anti-cancer metastasis effect of Jianpi Tiaoqi Decoction (JPTQ) on breast cancer-bearing mice by monitoring the effects of its on tumor proliferation, apoptosis, angiogenesis, epithelial to mesenchymal transition (EMT) process and regulation of immune microenvironment. Methods. The general phenotype of the Cancer-bearing mice was monitored. Bioluminescence-imaging was performed to assess the tumor status and the metastatic status of other organs. We investigated its mechanism of the effect through transcriptome analysis, Flow Cytometry(FCM) was used to analyze peripheralblood CD4+ T cells, spleen T helper 1 (Th1) cell, the proportion of MDSCs in lung. The changes of EMT process, vascular endothelial growth factor (VEGF) and Ki-67, Caspase-3 and Bcl-2 were detected by quantitative real time polymerase chain reaction (q-PCR), western blot (WB) or immunohistochemistry (IHC). Results. JPTQ inhibited the tumors proliferation and reduced lung metastasis. The transcriptome analysis of lung and tumor tissues indicated that EMT-related genes, angiogenesis, proliferation and apoptosis genes were regulated in JPTQ group, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis observed enrichment of immune-related pathways. FCM suggested that JPTQ could reduced the proportion of M-MDSCs in the lung, and increased peripheral blood CD4+ T cells and Th1 cells in spleen. The q-PCR, WB or IHC assay demonstrated that E-cadherin was up-regulated in lung and tumor tissue, and Snail was down-regulated, the expression of matrix metalloprotein-9(MMP-9)was down-regulated in lung tissue. IHC showed the down-regulation of Ki67 and VEGF in lung and tumo tissues. WB found that Cleved-Caspase3 was significantly up-regulated, while Bcl-2 was down-regulated. Conclution. JPTQ can inhibit proliferation, angiogenesis, promote apoptosis and improve the immune microenvironment, and reverse the EMT process to inhibit the proliferation and metastasis of TNBC.
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